This chapter integrates the structure and function of the airways, lungs, pleura, heart, great vessels and respiratory muscles, and applies that anatomy to the clinical reasoning needed for COPD, pericarditis and aortic dissection.
Thoracic Cage, Lungs and Pleura
The thorax contains 12 thoracic vertebrae, 12 pairs of ribs and the sternum. Ribs 1–7 attach directly to the sternum, ribs 8–10 attach via the costal margin, and ribs 11–12 are floating. The sternal angle (of Louis) marks the 2nd costal cartilage, the T4–T5 level, the tracheal bifurcation and the upper border of the pericardium. It is the main surface landmark for counting intercostal spaces.
The sternal angle marks the 2nd costal cartilage and the T4–T5 level, and is the main surface landmark for counting intercostal spaces.
The right lung has three lobes (upper, middle, lower) and two fissures. The left lung has two lobes (upper including the lingula, and lower), one oblique fissure and a cardiac notch.
Each lung is covered by a double-layered serous membrane:
- Visceral pleura adheres tightly to the lung surface and dips into the fissures.
- Parietal pleura lines the chest wall, diaphragm and mediastinum.
The potential space between the layers holds about 0.1–0.2 mL/kg of lubricating fluid. Intrapleural pressure is about −5 cmH₂O at end-expiration and falls to about −8 cmH₂O at the end of quiet inspiration. In pneumothorax, air enters this space, the lung recoils and the chest tube restores negative pressure. Drains are normally inserted in the "safe triangle" (4th–5th intercostal space, anterior to the mid-axillary line). Intercostal neurovascular bundles run along the inferior rib margin, so needles pass over the superior border of the rib.
Airway Anatomy
The upper airway comprises the nose, pharynx and larynx. The lower airway begins with the trachea, which is 10–12 cm long, has 16–20 C-shaped cartilage rings and runs from C6 to the carina at T4–T5. The trachea lies anterior to the oesophagus. The open posterior part of each ring is closed by the trachealis muscle, which abuts the oesophagus.
The right main bronchus is shorter (about 2.5 cm), wider and more vertical (about 25° from the midline) than the left (about 5 cm, 45°). Aspirated material and misplaced endotracheal tubes therefore usually enter the right lung. Common sites are the right lower lobe, and the posterior segment of the right upper lobe in supine patients.
The tracheobronchial tree divides about 23 times:
- Conducting zone (generations 0–16): no gas exchange; anatomical dead space about 150 mL (about 2 mL/kg).
- Respiratory zone (generations 17–23): respiratory bronchioles, alveolar ducts and alveoli.
Cartilage disappears at about the 11th generation, so small airways depend on radial traction from lung parenchyma to stay open. This is why emphysema (loss of tethering) causes expiratory airflow collapse. Bronchial smooth muscle, which contracts in asthma, is innervated by the vagus (constriction) and sympathetic β₂ receptors (dilatation).
Alveoli and Gas Exchange
The alveolus is the primary site of gas exchange. The lungs contain about 300 million thin-walled sacs, giving a surface area of 50–100 m². Type I pneumocytes cover about 95% of the surface. Type II pneumocytes secrete surfactant, which lowers surface tension and prevents collapse. The blood–gas barrier (alveolar epithelium, fused basement membrane, capillary endothelium) is only about 0.5 µm thick. Oxygen diffuses into the pulmonary capillaries, and CO₂ diffuses out. Pores of Kohn permit collateral ventilation between neighbouring alveoli.
Cardiac Anatomy and the Pericardium
The heart lies in the middle mediastinum, with its apex at the 5th intercostal space in the mid-clavicular line. It has four chambers: the right atrium and ventricle serve the pulmonary circuit, and the left atrium and ventricle serve the systemic circuit. Oxygen delivery follows this route: lungs → pulmonary veins → left atrium → mitral valve → left ventricle (wall 8–12 mm, versus 3–5 mm for the right) → aortic valve → aorta → tissues.
- Atrioventricular valves: tricuspid (right) and mitral (left).
- Semilunar valves: pulmonary and aortic.
- Coronary arteries: the left main divides into the LAD and circumflex, and the RCA arises from the right sinus. Coronary perfusion occurs mainly in diastole.
The pericardium has an outer fibrous layer and an inner serous layer. The serous layer has a parietal part lining the fibrous sac and a visceral part (epicardium) on the heart surface, with 15–50 mL of fluid between them. In acute pericarditis, inflamed layers rub together. The result is sharp pleuritic chest pain that worsens when supine or on inspiration and eases when leaning forward, a pericardial friction rub, and diffuse ST elevation with PR depression on ECG. Because the phrenic nerve supplies the pericardium, pain may refer to the trapezius ridge.
Heart Sounds and Auscultation
- S1 ("lub") is caused by mitral and tricuspid closure at the start of systole. It is loudest at the apex (5th intercostal space, mid-clavicular line).
- S2 ("dub") is caused by aortic and pulmonary closure at the start of diastole. It is loudest at the base (2nd intercostal space, right and left sternal borders).
S2 splits physiologically on inspiration, because increased venous return delays pulmonary closure. Auscultation sites are aortic (right 2nd ICS), pulmonic (left 2nd ICS), tricuspid (left lower sternal border) and mitral (apex). A new diastolic murmur at the left sternal edge suggests aortic regurgitation, which is relevant in proximal aortic dissection.
Respiratory Muscles and Resting Breathing Pattern
The diaphragm (phrenic nerve, C3–C5) is the primary muscle of quiet inspiration. It contracts, flattens and descends about 1.5 cm in quiet breathing (6–10 cm in maximal breathing). This increases vertical thoracic dimensions and displaces abdominal contents outward. The external intercostals and parasternals raise the ribs ("pump-handle" movement in the upper ribs, "bucket-handle" in the lower ribs).
A healthy resting pattern is diaphragmatic, with minimal upper chest movement, 12–20 breaths/min and an I:E ratio of about 1:2.
Accessory inspiratory muscles are the scalenes, sternocleidomastoid and upper trapezius. They are recruited in exercise, airflow obstruction or diaphragm weakness. Quiet expiration is passive elastic recoil. Active expiration uses the abdominals (transversus abdominis, obliques, rectus) and internal intercostals.
A healthy resting pattern is diaphragmatic: minimal upper chest movement, slight outward abdominal motion on inspiration, a rate of 12–20 breaths/min, tidal volume about 500 mL (minute ventilation 5–8 L/min), and an I:E ratio of about 1:2. In contrast, a patient with asthma or COPD may show apical breathing, visible sternocleidomastoid and scalene activity, prolonged expiration, and pursed lips.
Pathophysiology of COPD
COPD is persistent airflow limitation from small-airway disease (chronic bronchitis, with mucus hypersecretion and remodelling) and parenchymal destruction (emphysema). The usual cause is tobacco smoke or biomass exposure. Loss of elastic recoil and airway tethering causes expiratory flow limitation, air trapping and dynamic hyperinflation. The diaphragm becomes flattened and shortened, which puts it at a mechanical disadvantage and reduces its pressure-generating capacity. Accessory muscles take over, and the work of breathing and oxygen cost of breathing rise. Ventilation–perfusion mismatch produces hypoxaemia, and in advanced disease hypercapnia and cor pulmonale.
Spirometric diagnosis requires a post-bronchodilator FEV₁/FVC < 0.70. GOLD grades severity by FEV₁ % predicted: GOLD 1 ≥ 80%, GOLD 2 50–79%, GOLD 3 30–49%, GOLD 4 < 30%.
Pathophysiology of Aortic Dissection
An intimal tear allows blood to enter the media and create a false lumen. It may propagate to occlude branch vessels or rupture into the pericardium. Risk factors are hypertension (the most common), Marfan and Ehlers-Danlos syndromes, bicuspid aortic valve, cocaine use, pregnancy and heavy straining.
- Stanford A involves the ascending aorta and is a surgical emergency (DeBakey I and II).
- Stanford B arises distal to the left subclavian artery and is usually managed medically unless complicated (DeBakey III).
Clinical Presentation
COPD: chronic dyspnoea, cough, sputum, wheeze, barrel chest, Hoover's sign (paradoxical inward lower-rib movement on inspiration), pursed-lip breathing, tripod posture, reduced chest expansion, hyper-resonant percussion, distant breath sounds, and prolonged expiration.
Aortic dissection: abrupt, severe, "tearing" chest or interscapular pain, maximal at onset. Other findings are a systolic blood pressure difference > 20 mmHg between arms, pulse deficits, new aortic regurgitation murmur, syncope, focal neurological deficits and a widened mediastinum on chest X-ray. Diagnosis is by CT angiography.
Red flags requiring urgent medical referral: sudden tearing pain, a blood pressure differential > 20 mmHg between arms, SpO₂ < 88% at rest, new confusion or drowsiness (hypercapnia), pleuritic pain with fever or friction rub, and unilateral calf swelling.
Assessment
- Vital signs (normal resting): HR 60–100 bpm, BP < 120/80 mmHg, RR 12–20/min, SpO₂ 95–100%. Target SpO₂ in hypercapnic COPD is 88–92%.
- Observation and palpation: breathing pattern, accessory muscle use, thoracic shape and symmetry. Chest expansion (tape measure, axillary or xiphisternal level) is normally ≥ 2.5 cm.
- Auscultation: breath sounds (vesicular, bronchial, crackles, wheeze) and heart sounds at the four sites.
- Respiratory muscle strength: PImax (normal roughly ≥ 80–100 cmH₂O in men and ≥ 70 cmH₂O in women; < 60 cmH₂O suggests weakness).
- Dyspnoea scales: mMRC (0–4) and Borg CR10 (target 4–6 during exercise).
- Health status: COPD Assessment Test (CAT, 0–40; ≥ 10 indicates symptomatic disease).
- Exercise capacity: 6-minute walk test (MCID ≈ 30 m; < 350 m is associated with higher mortality) or incremental shuttle walk test (MCID ≈ 48 m).
- Peripheral strength: MRC grade 0–5 for key muscle groups, and handgrip dynamometry.
Physiotherapy Management
Staged protocols for stable COPD follow pulmonary rehabilitation principles.
Stage 1 – Education and breathing control (weeks 1–2):
- Positions of ease (forward lean with arms supported).
- Diaphragmatic breathing: 3 sets of 10 breaths, 2–3 times daily.
- Pursed-lip breathing with an inspiration:expiration ratio of 1:2–3.
- Airway clearance (active cycle of breathing technique) if sputum is present.
Stage 2 – Graded exercise (weeks 2–8):
- Supervised sessions 2–3 times per week for at least 6–8 weeks (ideally 20 or more sessions).
- Aerobic: 20–30 min continuous or interval walking or cycling at 60–80% of peak work rate or Borg 4–6, progressing by 5–10% when Borg falls below 4.
- Resistance: 1–3 sets of 8–12 repetitions at 60–70% 1RM, 2 days per week, for large muscle groups.
- Inspiratory muscle training (adjunct): start at about 30% PImax, 30 breaths once or twice daily, progressing by 5–10% weekly.
- Stop for SpO₂ < 85–88%, chest pain, dizziness, HR above the target ceiling or a fall in SBP.
Stage 3 – Maintenance: home-based programme with at least 150 min/week of moderate activity, self-management and an exacerbation action plan. Pulmonary rehabilitation should start within 4 weeks of discharge after an exacerbation.
Aortic dissection: it is a medical emergency, and physiotherapy has no role in the acute phase. After stabilisation or repair, it is usually delivered within a cardiac rehabilitation framework (guided by the treating team): keep SBP below the limit set by the team (commonly < 120–130 mmHg), keep exertion light to moderate (RPE 11–13), avoid Valsalva, isometric holds and heavy lifting, and monitor BP before and during sessions.
Evidence and Clinical Pearls
- Pulmonary rehabilitation improves dyspnoea, exercise capacity and quality of life, and reduces readmissions (Cochrane review, strong evidence).
- Hyperinflation shortens the diaphragm. Dyspnoea may improve more with forward-leaning positions than with "deep breathing".
- Sudden pain at rest in a hypertensive patient with a BP differential between arms must be treated as dissection until proven otherwise.
- A pneumothorax patient with a chest tube should not have the drain clamped or lifted above chest level.
- Always check which pleural layer is being discussed: visceral = lung, parietal = chest wall.
Summary
Knowing the surface landmarks, airway branching, the alveolar–capillary interface, cardiac chambers and valves, pericardial layers and respiratory muscle actions allows accurate interpretation of auscultation findings, breathing patterns and pain presentations. COPD is managed with staged breathing re-education, graded aerobic and resistance exercise, and self-management. Aortic dissection and pericarditis require recognition of red flags and careful, medically guided activity prescription.
References
- Global Initiative for Chronic Obstructive Lung Disease (GOLD). Global Strategy for the Diagnosis, Management, and Prevention of COPD: 2024 Report. GOLD; 2024.
- Spruit MA, Singh SJ, Garvey C, et al. An official ATS/ERS statement: key concepts and advances in pulmonary rehabilitation. Am J Respir Crit Care Med. 2013;188(8):e13–e64.
- Holland AE, Spruit MA, Troosters T, et al. An official ERS/ATS technical standard: field walking tests in chronic respiratory disease. Eur Respir J. 2014;44(6):1428–1446.
- Isselbacher EM, Preventza O, Hamilton Black J III, et al. 2022 ACC/AHA guideline for the diagnosis and management of aortic disease. Circulation. 2022;146(24):e334–e482.
- Adler Y, Charron P, Imazio M, et al. 2015 ESC guidelines for the diagnosis and management of pericardial diseases. Eur Heart J. 2015;36(42):2921–2964.
- McCarthy B, Casey D, Devane D, et al. Pulmonary rehabilitation for chronic obstructive pulmonary disease. Cochrane Database Syst Rev. 2015;(2):CD003793.
- Standring S, ed. Gray's Anatomy: The Anatomical Basis of Clinical Practice. 42nd ed. Elsevier; 2021.
- West JB, Luks AM. West's Respiratory Physiology: The Essentials. 11th ed. Wolters Kluwer; 2021.